# SEMA3B is associated with disease activity and infliximab response in IBD patients but does not contribute to the development of intestinal inflammation in vivo

## TL;DR

SEMA3B is linked to IBD disease activity and response to treatment, but it doesn't cause intestinal inflammation in mice.

## Contribution

The study identifies SEMA3B as a potential biomarker for IBD and evaluates its role in intestinal inflammation for the first time.

## Key findings

- SEMA3B expression is reduced in IBD patients compared to healthy controls.
- Low SEMA3B levels correlate with poor response to infliximab in UC patients.
- Administering Sema3B to mice did not affect the progression of DSS-induced colitis.

## Abstract

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder with increasing worldwide incidence and prevalence. While current treatment options alleviate part of the socioeconomic burden of this disease, new biomarkers and safer therapeutic approaches are needed to combat intestinal inflammation. Class-3 semaphorins (sema3A-3G) have emerged as important regulators of some biological functions underlying inflammation. For instance, SEMA3B protects against tissue damage in arthritis. However, the association of this protein with UC and its involvement in the onset of intestinal inflammation remains elusive.

To close that knowledge gap, we performed a comprehensive transcriptomic analysis of different patient cohorts. Moreover, we investigated the therapeutic efficacy of Sema3B in vivo.

Our findings revealed that the expression of SEMA3B was downregulated in IBD patients compared with healthy controls. Similarly, non-responder UC patients to infliximab showed reduced transcript levels of that class-3 semaphorin before receiving the treatment. Unfortunately, the administration of recombinant Sema3B to mice subjected to DSS-acute colitis did not modify the course of the disease.

Therefore, SEMA3B appears to be an interesting biomarker in the context of intestinal inflammation, which deserves further validation in larger cohorts. Nonetheless, based on our in vivo results, the implication of this factor in the development of colitis seems to be minimal.